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Cas Lek Cesk. 2002 Jun 21;141(12):363-70.
[Microdeletion syndromes]

[Article in Czech]

Seemanova E.

Oddeleni klinicke genetiky Ustavu biologie a lekarske genetiky 2. LF UK, Praha. eva.seemanovfmotol.cuni.cz

New high-resolution cytogenetical technique identified an increased number of terminal, interstitial and subtelomeric microdeletion as the etiology of many syndromes of multiple congenital anomalies, mental retardation and facial dysmorphy. A loss of contiguous genes shows a high phenotypical variability and at the same time it is significant for genetic prognosis. 1) Variability of clinical features depends on the size and pathogenetic mechanism of underlying deletion; 2) Dysmorphic face features are of a characteristic type and can be somatoscopically recognized; 3) Heart defects and mental retardation are common features of microdeletion syndromes; 4) New mutations represent the most common etiology of microdeletions; only 1 to 10% of mutations are transmitted from the parental gonadal mosaics, from the balanced translocation or from the same microdeletion in parents; 5) Recurrence risk is low, but it may be as high as 50% in individual cases of inherited mutation; 6) Genetic heterogeneity is high and the responsible genes can be located at different chromosomes (e.g. Di George syndrome due to mutation on 22q or 10q) and can also result from microdeletion or point mutation (in the Shprintzen syndrome 70% represent microdeletion and 30% point mutation at 22q11, in Rubinstein-Taybi syndrome 10% cases result from microdeletions and 90% from point mutations); 7) Population incidence of microdeletions is high (1:4000 to 1:30,000) because their etiologic mechanism is related to the common unequal crossing over; 8) Imprinting plays a role in some cases, e.g. Prader-Willi syndrome results from nullisomy of paternal 15q12 chromosome, Angelman syndrome is related to that of maternal 15q12 chromosome; 9) Prenatal prevention of the high risk familial chromosomal rearrangements is feasible since the 12th gestation week.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12238021&dopt=Abstract

Presse Med. 2002 Aug 24;31(27):1263-5.
[Digestive malacoplakia]

[Article in French]

Ennibi K, Mikdame M, Bahrouch L, Chaari J, Toloune F, Archane MI.

Service de medecine interne A. Hopital militaire d'instruction Mohammed V, Rabat, Maroc. kennibahoo.fr

INTRODUCTION: Malacoplakia, a chronic granulomatous disease, rarely involves the digestive tube and, when it does, takes on a pseudotumoral aspect. OBSERVATION: A 37 year-old man was hospitalized for chronic diarrhea that had progressed over 15 years. He exhibited an edematous-ascitic syndrome and bilateral pleurisy together with, biologically, a malabsorption syndrome. The endoscopic examinations (fibroscopy and colonoscopy) revealed polypoid tumor-like formations. An image of tumoral stenosis of the sigmoid-colic junction was revealed on barite lavage. Histological examination of the surgical sample (wide left colectomy of one third of the transverse) was suggestive of malacoplakia (histiocytes with characteristic Michaelis-Gutmann bodies). DISCUSSION: Malacoplakia is an inflammatory disease predominantly affecting the urogenital tract. Other organs can be involved. Its clinical symptomatology is highly disparate. The interest of this disease is in its pathogenesis, on which, in fact, its treatment is based.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12238271&dopt=Abstract

J Neuropathol Exp Neurol. 2002 Nov;61(11):968-74.
Upregulation of HSP27 in a transgenic model of ALS.

Vleminckx V, Van Damme P, Goffin K, Delye H, Van Den Bosch L, Robberecht W.

Dept. of Neurology, University of Leuven, Medical School, Belgium.

Mutations of the SOD1 gene underlie 1 form of familial amyotrophic lateral sclerosis (ALS). Their pathogenic mechanism remains uncertain, but is thought to involve oxidative stress and abnormal protein aggregation, 2 processes known to induce heat shock proteins (HSPs). We studied the expression of 3 HSPs (alphaB-crystallin, HSP27, and HSP70) in transgenic mice overexpressing human mutant (G93A and G37R) SOD1, using a combination of immunohistochemistry and immunoblotting. Quantitative Western blot analysis demonstrated alphaB-crystallin and HSP27 to be upregulated in the spinal cord of mutant SOD1 mice compared to mice overexpressing wild-type SOD1. HSP70 levels were normal. Immunocytochemical studies of the ventral horn of the spinal cord demonstrated HSP27 to be localized in the nucleus of neurons and glial cells in presymptomatic and early symptomatic animals, where it often was punctate in pattern. In the later stages of the disease, HSP27 was predominantly present in the cytoplasm of reactive glial cells. The early nuclear localization was confirmed by Western blot analysis of spinal cord nuclear and cytoplasmic fractions. In contrast to HSP27, alphaB-crystallin was localized exclusively in the cytoplasm of reactive glial cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12430713&dopt=Abstract

Plant J. 2003 Jan;33(2):245-57.
Susceptible to intolerance--a range of hormonal actions in a susceptible Arabidopsis pathogen response.

O'Donnell PJ, Schmelz EA, Moussatche P, Lund ST, Jones JB, Klee HJ.

Department of Horticultural Sciences, University of Florida, Gainesville, FL 32611, USA.

Ethylene and salicylic acid (SA) are key intermediates in a host's response to pathogens. Previously, we have shown using a tomato compatible interaction that ethylene and SA act sequentially and are essential for disease symptom production. Here, we have examined the relationship between the two signals in the Arabidopsis-Xanthomonas campestris pv. campestris (Xcc) compatible interaction. Preventing SA accumulation by expression of the nahG gene reduced subsequent ethylene production and altered the development of disease symptoms, with plants showing no visible chlorosis. The ethylene insensitive lines, etr1-1 and etr2-1, on the other hand, accumulated SA and exhibited normal but precocious symptom development. Therefore, Arabidopsis, like tomato, was found to exhibit co-operative ethylene and SA action for the production of disease symptoms. However, in Arabidopsis, SA was found to act upstream of ethylene. Jasmonic acid and indole-3-acetic acid levels were also found to increase in response to Xcc. In contrast to ethylene, accumulation of these hormones was not found to be dependent on SA action. These results indicate that the plants response to a virulent pathogen is a composite of multiple signaling pathways.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12535339&dopt=Abstract [PubMed - in process]

J Neurochem. 2002 Dec;83(6):1509-24.
Disruption of neurogenesis by amyloid beta-peptide, and perturbed neural progenitor cell homeostasis, in models of Alzheimer's disease.

Haughey NJ, Nath A, Chan SL, Borchard AC, Rao MS, Mattson MP.

Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA.

Neurogenesis occurs in the adult mammalian brain and may play roles in learning and memory processes and recovery from injury, suggesting that abnormalities in neural progenitor cells (NPC) might contribute to the pathogenesis of disorders of learning and memory in humans. The objectives of this study were to determine whether NPC proliferation, survival and neuronal differentiation are impaired in a transgenic mouse model of Alzheimer's disease (AD), and to determine the effects of the pathogenic form of amyloid beta-peptide (Abeta) on the survival and neuronal differentiation of cultured NPC. The proliferation and survival of NPC in the dentate gyrus of the hippocampus was reduced in mice transgenic for a mutated form of amyloid precursor protein that causes early onset familial AD. Abeta impaired the proliferation and neuronal differentiation of cultured human and rodent NPC, and promoted apoptosis of neuron-restricted NPC by a mechanism involving dysregulation of cellular calcium homeostasis and the activation of calpains and caspases. Adverse effects of Abeta on NPC may contribute to the depletion of neurons and cognitive impairment in AD.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12472904&dopt=Abstract

The average human scalp is covered by approximatey 100,000 hair follicles. Each hair undergoes hair cycle and normally 50-100 hairs randomly fall out a day, which is unnoticeable because lost hair is replaced by as many new hairs springing up daily. Hair loss results from the fall out of hair from the hair follicle. Alopecia or excessive, premature hair loss is the condition caused by many factors. Loss of hair itself does not pose critical health problems because biological role of human hair is relatively marginal. Hair on our scalp protects the head from mechanical shock, heat loss, and exposure to UV-light. The eyelashes and eyebrowes protect the eyes, and hair in the ear canal or the nasal passages help filter out particles and pathogens, thus protecting our internal organs. However, hair does play important social role: it is one of the major determinants of our appearance and identity in daily life. Fullness of hair also implicates or manifests physical integrity and youthfulness of the person. Losing hair could have more than just emotional impacts on individuals. The hair is a unique organ that goes through a characteristic cycle consisting of an immature phase, a growing phase called anagen, a transitional phase between the growing phase and the resting phase called catagen, and finally a resting phase called telogen in which the hair stops growing, waiting to fall out. 85-90% of hairs on our body are in anagen phase or growing phase, which lasts anywhere from two to five years. This phase is followed by a short regression phase, or catagen, which lasts 2-3 weeks. Approximately 1% of hair follicles are in catagen. Approximately 10-15% of hair follicles are in the resting phase, the telogen, which lasts about 3-5 months. Hair follicles typically goes through 10-20 asynchronous cycles during the lifetime. Persistent loss of more than 150 hairs would consist a state of hair loss, or alopecia, albeit it could be temporary.

DHEA is a natural hormone, and it is produced in our body by the adrenal glands. DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells. Our bodies produce decreasing amount of DHEA as we get older. various health benefits: To deter aging, improve sexual function/erectile dysfunction, treat cognitive decline, enhance athletic performance, facilitate weight loss, improve strength, prevent osteoporosis, enhance immunomodulation for rheumatic conditions, and treat depression.

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